Melatonin has an ergogenic effect but does not prevent inflammation and damage in exhaustive exercise

It is well documented that exhaustive physical exercise leads to inflammation and skeletal muscle tissue damage. With this in mind, melatonin has been acutely administered before physical exercise; nevertheless, the use of melatonin as an ergogenic agent to prevent tissue inflammation and damage remains uncertain. We evaluated the effects of melatonin on swimming performance, muscle inflammation and damage and several physiological parameters after exhaustive exercise at anaerobic threshold intensity (iLAn) performed during light or dark circadian periods. The iLAn was individually determined and two days later, the animals performed an exhaustive exercise bout at iLAn 30 minutes after melatonin administration. The exercise promoted muscle inflammation and damage, mainly during the dark period and the exogenous melatonin promoted a high ergogenic effect. The expressive ergogenic effect of melatonin leads to longer periods of muscle contraction, which superimposes a possible melatonin protective effect on the tissue damage and inflammation5CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP305650/2009- 22009/08535-5; 2011/13226-1; 2012/20501-

Aerobic capacity of wistar rats: the effects of training and physical detraining at middle-aged

It has been shown that engaging in regular physical exercise yields short- and long-term health benefits, primarily by mitigating the risk for cardiovascular disease, but little information is known about physical deconditioning at aging process. The aim of the present study was to analyze the aerobic capacity, through maximal lactate steady state (MLSS), in Wistar rats of different ages (2,4, 6 e 12 months ) and physical conditioning deconditioning responses in middle-aged rats. The results were significant for weight gain in the sedentary (588 ± 71 g) and detraining animals (576 ± 62 g) at 12 months, whereas the conditioned group maintained their original body weights – BW (515 ± 72 g), similar at four (455 ±17 g) and six months of age (471 ± 37 g). MLSS decreased with age (2 months sedentary (8.4 ± 1% Body Weight, 4 months sedentary (6.4 ± 0.6% BW), 6 months sedentary (5.8 ± 1% BW), 12 months sedentary (5.1 ± 0.7% BW), but physical exercise was effective in attenuating the age-related loss of aerobic capacity after 12 months (5.8 ± 1.3% BW). The physical detraining was (5.3 ± 0.4% BW) was similar at 12 months trained. The physical training in long term protected against the increased of the body weight and fat depots caused by aging, but, this effect was found by deconditioning physical. Additionally, the physical training attenuated the aerobic capacity loss due to aging process and this effect was maintained after detraining physical.Tem sido demonstrado que o engajamento em exercícios físicos regulares gera benefícios para a saúde a curto e a longo prazo, principalmente a redução do risco de doença cardiovascular, mas pouco se sabe sobre o destreinamento físico no processo de envelhecimento. O objetivo do presente estudo foi analisar a capacidade aeróbia, através da máxima fase estável de lactato (MFEL), em ratos Wistar de diferentes idades e em resposta ao treinamento e ao destreinamento físico em ratos de meia-idade. Os resultados foram significativos para o ganho de peso corporal no grupo sedentário (588 ± 71 g) e animais destreinados com 12 meses (576 ± 62 g), enquanto o grupo treinado manteve o peso corpo semelhante aosanimais – PC (515 ± 72 g), do grupo de quatro meses (455 ± 17 g) e seis meses de idade (471 ± 37 g). Como medida da capacidade aeróbia, a MFEL diminuiu com a idade (2 meses sedentários (8,4 ± 1% PC), 4 meses sedentários (6,4 ± 0,6% PC), 6 meses sedentários (5,8 ± 1% PC), 12 meses sedentários (5.1 ± 0,7% PC), mas o exercício físico foi eficaz em atenuar a perda da capacidade aeróbia relacionada com a idade, o grupo 12 meses treinados (5,8 ± 1,3% PC) e o grupo destreinado (5,3 ± 0,4% PC) tiveram resultados semelhante na capacidade aeróbia. O treinamento físico de longo prazo protege contra o aumento do peso corporal e o aumento de depósitos de gordura causada pelo envelhecimento. Porém, este efeito foi abolido pelo destreinametno físico. Além disso, o treinamento físico preveniu a diminuição da capacidade aeróbia, devido ao processo de envelhecimento e este efeito foi mantido após destreinamento físico

Exercício físico, ingestão de frutose e marcadores da síndrome metabólica em modelo experimental

Metabolic Syndrome has become serious medical-social problem in developed and development country and the excessive fructose consumption in the occidental diet has a major role in this question. This way, it has been a great interest the development of procedures more effectives to prevent and treat this disease. The non-alcoholic fatty liver disease (NAFLD) emerges as a syndrome component and can be related to the development of insulin resistance. Once human studies have many limitations it is necessary the use of animal models adequate to this disease study. This research aims to investigate the potential effects of the physical exercise in the pathophysiology of fructose-induced metabolic syndrome, oxidative stress and inflammation. The first step aimed to analyses the effects of fructose-rich diet in metabolic syndrome markers. We used Wistar rats (120 days), separated in two groups, according to the diet: control (balanced Labina ® dieta) and fructose-rich diet (60% of caloric content provided by fructose). The animals fed on a fructose rich diet for 60 days (120-180 days). At the end of experiment, they were euthanized to determine in order: the glucose tolerance, insulin sensitivity, insulin levels, biomarkers of nonalcoholic fatty liver disease, biomarkers of oxidative stress and liver histology. The animals fed on fructose rich-diet showed lower glucose tolerance, insulin sensitivity, hiperinsulinemia, raises on serum glucose and triglycerides, higher AST/ALT ratio, fat accumulation in the liver and in the mesenteric adipose tissue, a reduction in the anti-oxidant system activities and higher levels of TBARs. The second step consisted to evaluate the effects of three exercise protocols in Wistar rats (120 days) on metabolic syndrome markers. Quarter of the animals were kept sedentary (C) during all the experiment (120-180 days); a quarter animals trained in the aerobic protocol (A) (80% of minimal lactate) 1h day, 5 days week,...A síndrome metabólica tornou-se grave problema médico-social tanto em países desenvolvidos quanto em desenvolvimento e o consumo excessivo de frutose na dieta parece ter papel importante nessa questão. Dessa forma, é de grande interesse o desenvolvimento de procedimentos mais efetivos para prevenção e tratamento desta doença. Um dos procedimentos que merece investigação é o exercício físico. O presente estudo visou avaliar os efeitos singulares de três protocolos de exercício físico na prevenção e tratamento de complicações metabólicas desencadeadas por uma dieta rica em frutose. Numa primeira série de experimentos, visou-se analisar os efeitos de uma dieta rica em frutose sobre biomarcadores hepáticos e da síndrome metabólica em ratos. Foram utilizados ratos da linhagem Wistar que a partir dos 120 dias de idade, foram separados em dois grupos, conforme a dieta: controle (ração comercial para roedores labina ®) e frutose (dieta semipurificada com 60% de frutose). Ao final foram analisados tolerância à glicose (teste de tolerância oral à glicose), sensibilidade periférica à insulina (teste de tolerância à insulina), marcadores de esteatose hepática não alcoólica (EHNA) (concentrações séricas de alanina aminotransferase - ALT, aspartato aminotransferase - AST). Foram, ainda, determinados no fígado: concentrações de lipídios totais e de triglicerídeos, taxa de lipogênese hepática, biomarcadores do sistema de defesa antioxidante (atividade das enzimas catalase - CAT e superóxido dismutase - SOD) e de peroxidação lipídica (substâncias que reagem ao ácido tiobarbitúrico – TBARs) e histologia hematoxilina-eosina. Os animais alimentados com dieta rica em frutose apresentaram uma redução na tolerância à glicose, hiperinsulinemia, resistência à insulina, aumento na glicose e nos triglicerídeos circulantes, aumento na relação AST/ALT, acúmulo de gordura no fígado e no tecido adiposo..

Exercício físico, dieta rica em frutose e marcadores da síndrome metabólica em ratos

O presente estudo visou analisar os efeitos do exercício de caráter aeróbio sobre marcadores de esteatose hepática não alcoólica (EHNA), tolerância à glicose, sensibilidade à insulina e capacidade aeróbia de ratos mantidos em dieta rica em frutose. Foram utilizados ratos da linhagem Wistar que foram separados em dois grupos, conforme a dieta recebida: controle (dieta balanceada AIN-93 G) e frutose (dieta com 60% de frutose). Esses animais foram submetidos a testes de máximo estado estável de lactato (MEEL) para a identificação da transição metabólica aeróbia/anaeróbia durante exercício de natação aos 28, 90 e 120 dias de idade. Um terço dos animais de cada grupo foi submetido ao treinamento por natação, em intensidade equivalente ao MEEL, 1 h/dia, 5 dias/semana dos 28 aos 120 dias (protocolo precoce), outro terço foi submetido ao mesmo treinamento dos 90 aos 120 dias (protocolo tardio) e os restantes, permaneceram sedentários. As principais análises efetuadas foram: capacidade aeróbia (MEEL), tolerância à glicose (oGTT); sensibilidade periférica à insulina (ITT); marcadores de EHNA (concentrações séricas de alanina aminotransferase [ALT], aspartato aminotransferase [AST], fosfatase alcalina e as concentrações hepáticas de lipídios [totais] e concentração de triglicerídeos séricos [TG]). O treinamento precoce reduziu a carga de trabalho no MEEL do lactato dos animais alimentados com ambas as dietas. Já o treinamento tardio aumentou essa carga de trabalho nos ratos alimentados com dieta controle. O treinamento tardio, também reduziu a área sob a curva de glicose durante GTT nos ratos controle. A dieta rica em frutose diminuiu a sensibilidade à insulina dos animais. No entanto, o protocolo de exercício tardio foi eficiente em melhorar esse aspecto. Não houve diferença entre os grupos nas concentrações de ALT séricas, no entanto...This study aimed to analyze the effects of aerobic exercise on markers of non alcoholic steatohepatitis (EHNA), glucose tolerance, insulin sensitivity and aerobic capacity of rats kept on a fructose rich diet. We used rats of Wistar strain which were separated into two groups according to diet: control (balanced diet AIN-93 G) and fructose (diet with 60% fructose). These animals were tested for maximum lactate steady state (MEEL) to identify the aerobic / anaerobic metabolic transition exercise during swimming at 28, 90 and 120 days of age. One third of the animals in each group was subjected to swimming training at intensity equivalent to MEEL, 1 h / day, 5 days / week from 28 to 120 days (early protocol), another third was submitted to the training from 90 to 120 days (late Protocol) and the others remained sedentary. The main tests performed were: aerobic capacity (MEEL), glucose tolerance (oGTT) peripheral sensitivity to insulin (ITT), markers of EHNA (serum alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase and hepatic concentrations of lipids [total], and concentration of serum triglycerides [TG]). The early protocol reduced the workload on MEEL in animals fed both diets. On the other hand, the later training increased work load in rats fed control diet. The later training, also reduced the areas under the glucose curve during oGTT in control rats. The fructose rich diet decreased sensitivity to insulin in these animals. However, the later exercise protocol was efficient in improving this. There was no difference between groups in concentrations of serum ALT, but the concentrations of AST increased in the fructose sedentary group compared to other groups. There was an increase in liver lipids of animals fed with fructose rich diet and sedentary. Serum concentrations of triglycerides were increased in high fructose trained groups compared with... (Complete abstract click electronic access below)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES

Acute physical exercise increases leptin‐induced hypothalamic extracellular signal‐regulated kinase1/2 phosphorylation and thermogenesis of obese mice

The obesity is a result of energy imbalance and the increase in thermogenesis seems an interesting alternative for the treatment of this disease. The mechanism of energy expenditure through thermogenesis is tightly articulated in the hypothalamus by leptin. The hypothalamic extracellular signal‐regulated kinase‐1/2 (ERK1/2) is a key mediator of the thermoregulatory effect of leptin and mediates the sympathetic signal to the brown adipose tissue (BAT). In this context, physical exercise is one of the main interventions for the treatment of obesity. Thus, this study aimed to verify the effects of acute physical exercise on leptin‐induced hypothalamic ERK1/2 phosphorylation and thermogenesis in obese mice. Here we showed that acute physical exercise reduced the fasting glucose of obese mice and increased leptin‐induced hypothalamic p‐ERK1/2 and uncoupling protein 1 (UCP1) content in BAT ( P < 0.05). These molecular changes are accompanied by an increased oxygen uptake (VO 2) and heat production in obese exercised mice ( P < 0.05). The increased energy expenditure in the obese exercised animals occurred independently of changes in spontaneous activity. Thus, this is the first study demonstrating that acute physical exercise can increase leptin‐induced hypothalamic ERK1/2 phosphorylation and energy expenditure of obese mice1201697704CNPQ - Conselho Nacional de Desenvolvimento Científico e TecnológicoFAPESP – Fundação de Amparo à Pesquisa Do Estado De São Paulo306535/2017‐32016/18488‐8OCR

Transcriptional and molecular pathways activated in mesenteric adipose tissue and intestinal mucosa of Crohn's disease patients

FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCrohn’s disease (CD) is a chronic inflammatory disorder, characterized by cytokine imbalance and transcription signaling pathways activation. In addition, the increase of mesenteric adipose tissue (MAT) near the affected intestinal area is a hallmark of C20171110FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOsem informaçã

Acute Exercise Decreases Trb3 Protein Levels In The Hypothalamus Of Obese Rats.

To evaluate the effects of acute exercise on the TRB3 protein levels and interaction between TRB3/Akt proteins in the hypothalamus of obese rats. In addition, we evaluated the relationship between TRB3 and endoplasmic reticulum stress (ER stress) and verified whether an acute exercise session is able to influence these processes. In the first part of the study, the rats were divided into three groups: control (lean) - fed with a standard rodent chow, DIO - fed with a high fat diet and DIO submitted to a swimming acute exercise protocol (DIO-EXE). In the second part of the study, we used other three groups: control (lean) receiving an intracerebroventricular (i.c.v.) infusion of vehicle, lean receiving an i.c.v. infusion of thapsigargin, and lean receiving an i.c.v infusion of thapsigargin and performing an acute exercise session. Four hours after the exercise session, the food intake was measured and the hypothalamus was dissected and separated for subsequent protein analysis by immunoblotting and Real Time PCR. The acute exercise session reduced the TRB3 protein levels, disrupted the interaction between TRB3/Akt proteins, increased the phosphorylation of Foxo1 and restored the anorexigenic effects of insulin in the hypothalamus of DIO rats. Interestingly, the suppressive effects of acute exercise on TRB3 protein levels may be related, at least in part, to the decrease of ER stress (evaluated though pancreatic ER kinase phosphorylation - pPERK and C/EBP homologous protein - CHOP protein levels) in the hypothalamus. In conclusion, the reduction of hypothalamic TRB3 protein levels mediated by exercise may be associated with the reduction of ER stress. These data provided a new mechanism by which an acute exercise session improves insulin sensitivity in hypothalamus and restores food intake control in obesity